The importance of cell-mediated immunity in pathophysiology of animal models of uveitis has been demonstrated. Its significance in most human uveitides is unclear. This lack of clarity is due in part to lack of resolution of two issues: (1) whether the CMI demonstrated to antigens derived from ocular tissues is an important etiologic mechanism in human uveitis or merely secondary to tissue injury; (2) if cellular reactivity is of biological significance, which ocular tissue antigens are important in production of uveitis. Rosette and lymphocyte stimulation assays have been demonstrated to be sensitive measures of some parameters of CMI. In some human states alterations in T-cell number and function have been observed; and are of diagnostic and prognostic significance. In patients with uveitis, parameters of non-specific CMI have been measured using these assays to determine whether alterations in immune status exist in uveitis; and whether these alterations are of diagnostic and prognostic value. Many patients with chorioretinitis have damaged retinal pigment epithelium. Isotope release assay and leukocyte migration inhibition assay are used to determine whether patients have cellular reactivity to antigens derived from retinal pigment epithelium; whether changes in reactivity occur with alterations in disease status. A study of immunosuppression as a treatment modality in patients with severe uveitis is currently ongoing. The above assays are used to monitor patients' immunologic status to determine the importance of CMI in these diseases, and whether some parameters of CMI correlate with changes in disease status on therapy or prognosis. Delineation of CMI in patients with uveitis will increase our understanding of the patho-physiology of this group of diseases, and possibly be of diagnostic, prognostic, and therapeutic value.